Hu · Gut microbes 2025 · Preclinical animal and in vitro study with human observational cohort validation · n=?

Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate.

Cited 26 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical animal and in vitro mechanistic study with supplementary human observational correlation

PubMed 40223164 · doi:10.1080/19490976.2025.2486515 · record verified 2026-08-30

What was done

Researchers investigated whether time-restricted feeding (TRF) mitigates sepsis-associated liver injury using septic mouse models, germ-free mice, liver-specific Hmgcs2 and Lpin1 knockout mice, and cultured AML12 hepatocytes. They utilized 16S rRNA sequencing, Q200 targeted metabolomics, and transcriptomic profiling. In addition, serum 3-hydroxybutyrate (3-HB) levels and gut microbiota were measured in a cohort of septic human patients to evaluate clinical correlation and diagnostic predictive capacity.

What was found

TRF enriched gut *Lactobacillus murinus*, which was otherwise depleted in septic mice. Live *L. murinus* supplementation raised circulating 3-HB and alleviated septic liver damage, an effect lost when hepatic 3-HB synthesis was blocked via *Hmgcs2* knockout. Mechanistically, 3-HB activated the PI3K/AKT/mTOR/LPIN1 pathway, reducing ACSL4, MDA, lipid peroxides (LPO), and intracellular Fe2+, thereby blocking hepatocyte ferroptosis. In septic patients, serum 3-HB correlated positively with *L. murinus* and negatively with liver injury markers, predicting septic liver injury with an area under the curve (AUC) of 0.8429.

Why it matters

This study links a dietary regimen (TRF) to gut microbial modulation and metabolite signaling (3-HB) that directly prevents hepatocyte ferroptosis during sepsis, identifying 3-HB as a potential therapeutic candidate and diagnostic biomarker.

Limits

The abstract omits exact sample sizes for both animal experiments and human cohorts. The therapeutic administration of TRF was evaluated in rodents rather than human trials, and human findings are limited to observational biomarker correlations without demonstrating that dietary timing modifies clinical sepsis outcomes.

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